The Effects Of 4-amino-2-trifluoromethyl-phenyl Retinate On Human Gastric Cancer Cell SGC7901 With Endocan Overexpression And Its Molecular Mechanisms

Objective A preliminary study to investigate the influence of 4-amino-2-trifluoromethyl-phenyl retinate(ATPR)on the apoptosis and migration of gastric cancer cell SGC7901 with endocan overexpression and discuss the potential molecular mechanisms.Methods Gastric cancer cell SGC7901 with endocan overexpression and SGC7901 cell were treated with ATPR.MTT assay was used to measure cell proliferation,the cell apoptosis was detected by Hoechst staining and trypan blue staining.Cell migration ability was analyzed by Wound-healing assay.Western blot was used to detect the expression of apoptosis-related proteins(Caspase-3?Bax?Bcl-2?p53),migration-related proteins(MMP-9?N-cadherin?E-cadherin)and the phosphorylation level of MAPK signaling pathway proteins.Results After treated with ATPR,SGC7901 cells growth was inhabited in a dose-dependent manner.Hoechst staining and trypan blue staining have shown ATPR induced the apoptosis of gastric cancer cell SGC7901 with endocan overexpression.Hoechst staining results were observed under inverted microscope,when compared with wild type SGC7901 cells,the cell nucleus of SGC7901 cells with endocan overexpression is hyperchromatic and apoptotic.However,SGC7901 cells with endocan overexpression which treated with ATPR showed more hyperchromatic nucleus and apoptotic.Trypan blue staining displayed that,after ATPR treatment,the proportion of dead cells dyed blue in SGC7901 cells with endocan overexpression is increasing.The results of wound-healing assay showed that ATPR inhibited the migration of gastric cancer SGC7901 cells.The results of Western blot showed that ATPR promoted the expression of endocan.And in the treatment group of OE-SGC7901,the expression of cleaved-Caspase-3?p53?CHOP?E-cadherin?pp38 were significantly increased,the expression of Bcl-2/Bax?MMP-9?N-cadherin?p-Src?GRP78?p-ERK were decreased.Conclusions Endocan induced apoptosis of gastric cancer cell SGC7901 and inhibited its migration.ATPR can increase the expression of endocan thus increase the effects of endocan induced apoptosis and migration inhibition.The possible molecular mechanisms of apoptosis inducing and migration inhibiting effects are associated with the changed expression of apoptosis-related proteins and migration-related proteins regulated by ERK and p38 MAPK signaling pathway.